Subject(s)
ATP-Binding Cassette Transporters/genetics , Bile Acids and Salts/metabolism , Cholestasis, Intrahepatic/diagnosis , Craniocerebral Trauma/diagnosis , ATP Binding Cassette Transporter, Subfamily B, Member 11 , Child Abuse/diagnosis , Cholestasis, Intrahepatic/genetics , Cholestasis, Intrahepatic/therapy , Diagnosis, Differential , Female , Hematoma, Subdural/diagnosis , Hematoma, Subdural/etiology , Humans , Infant , Liver Transplantation , Point Mutation , Retinal Hemorrhage/diagnosis , Retinal Hemorrhage/etiologyABSTRACT
BACKGROUND: Cancer stem cells (CSCs) are thought to be a critical subpopulation in tumor development, progression, metastasis and recurrence, and the identification of these cells is an initial step in understanding their role in oncogenesis and in seeking valuable markers for diagnosis or development of targeting therapeutics. AIMS: To identify CSCs in hepatocellular carcinoma (HCC) specimens and define their tissue specificity. METHODS: Immunohistochemical staining of CSC markers: CD44, CD90, CD133 and aldehyde dehydrogenase (ALDH) was performed in 25 HCC specimens, 4 hepatoblastomas, 8 peri-malignant tissues, and 19 cases of viral hepatitis. RESULTS: The positivity of CD44 staining in HCC specimens was significantly lower than in viral hepatitis specimens. The positive rate of CD133 in HCC was similar to viral hepatitis specimens. CD133(+) cells were largely localized to ALDH-positive cells in HCC as revealed by confocal microscopy. In contrast, the co-expression of both markers was visualized within vessels or in the portal areas in viral hepatitis. Moreover, among 7 liver specimens adjacent to HCC tissue, 3-6 samples were positive for CD44, CD90, CD133 and ALDH, especially in dysplastic cells. One of 4 hepatoblastoma cases was positive for all these markers; whereas, the other three specimens were negative for all these CSC markers. CONCLUSIONS: In HCC and dysplastic tissues, clusters of CD133(+)/ALDH(high) cells were identified. The use of cancer stem cell markers to screen tissues with chronic liver diseases provides limited guidance in the identification of malignant cells.
Subject(s)
Biomarkers, Tumor/metabolism , Carcinoma, Hepatocellular/metabolism , Hepatitis, Viral, Human/metabolism , Liver Neoplasms/metabolism , Neoplastic Stem Cells/metabolism , AC133 Antigen , Adult , Aged , Aldehyde Dehydrogenase/metabolism , Antigens, CD/metabolism , Carcinoma, Hepatocellular/pathology , Female , Glycoproteins/metabolism , Hepatitis, Viral, Human/pathology , Humans , Hyaluronan Receptors/metabolism , Immunoenzyme Techniques , Liver/metabolism , Liver/pathology , Liver Neoplasms/pathology , Male , Middle Aged , Neoplastic Stem Cells/pathology , Peptides/metabolism , Thy-1 Antigens/metabolism , Young AdultABSTRACT
Eosinophilic gastroenteritis (EG) is an uncommon disease characterized by focal or diffuse eosinophilic infiltration of the gastrointestinal tract, and is usually associated with dyspepsia, diarrhea and peripheral eosinophilia. Diffuse gastrointestinal tract and colonic involvement are uncommon. The endoscopic appearance may vary from normal to mucosal nodularity and ulceration. Gastrointestinal obstruction is unusual and is associated with predominantly muscular disease. We present five unusual cases of EG associated with gastric outlet and duodenal obstruction. Two cases presented with acute pancreatitis and one had a history of pancreatitis. Four cases responded well to medical therapy and one had recurrent gastric outlet obstruction that required surgery. Four out of the five cases had endoscopic and histological evidence of esophagitis and two had colitis. Two patients had ascites. These cases reaffirm that EG is a disorder with protean manifestations and may involve the entire gastrointestinal tract. Gastric outlet and/or small bowel obstruction is an important though uncommon presentation of EG. It may also present as esophagitis, gastritis with polypoid lesions, ulcers or erosions, colitis and pancreatitis and may mimic malignancy.
Subject(s)
Eosinophilia/immunology , Eosinophilia/physiopathology , Gastroenteritis/immunology , Gastroenteritis/physiopathology , Adult , Aged , Eosinophilia/diagnosis , Eosinophilia/therapy , Female , Gastroenteritis/diagnosis , Gastroenteritis/therapy , Gastrointestinal Agents/therapeutic use , Humans , Male , Middle Aged , Weight LossABSTRACT
Infection with the human immunodeficiency virus (HIV) is often associated with the acquired immunodeficiency syndrome (AIDS), and wasting is one of the defining clinical features of AIDS. Muscular weakness due to myopathy may develop at any stage of HIV infection. We report two illustrative cases of HIV-associated myopathies. One was due to inflammatory myosits most likely directly related to the HIV infection, and the other was most likely the result of mitochondrial damage due to zidovudine, a nucleoside analogue commonly used in treating HIV infection. Biopsies from both patients showed alterations of myofiber structures, of varying severity, culminating in necrosis, lipid droplets, and lymphoplasmocytic inflammatory response. The zidovudine-treated patient also showed distinctive mitochondrial changes, predominantly enlargement, variation in shape and size, and disorganization of the cristae. These two types of HIV-associated inflammatory myopathies are reviewed, along with other HIV-associated myopathies, including HIV wasting syndrome, nemaline rod myopathy, pyomyositis, rhabdomyolysis, cardiomyopathy, and other miscellaneous myopathies associated with HIV infection.
